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Title: Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signaling pathways in SKH-1 mice skin

Abstract

Extensive exposure of solar ultraviolet-B (UVB) radiation to skin induces oxidative stress and inflammation that play a crucial role in the induction of skin cancer. Photochemoprevention with natural products represents a simple but very effective strategy for the management of cutaneous neoplasia. In this study, we investigated whether blackberry extract (BBE) reduces chronic inflammatory responses induced by UVB irradiation in SKH-1 hairless mice skin. Mice were exposed to UVB radiation (100 mJ/cm{sup 2}) on alternate days for 10 weeks, and BBE (10% and 20%) was applied topically a day before UVB exposure. Our results show that BBE suppressed UVB-induced hyperplasia and reduced infiltration of inflammatory cells in the SKH-1 hairless mice skin. BBE treatment reduced glutathione (GSH) depletion, lipid peroxidation (LPO), and myeloperoxidase (MPO) in mouse skin by chronic UVB exposure. BBE significantly decreased the level of pro-inflammatory cytokines IL-6 and TNF-α in UVB-exposed skin. Likewise, UVB-induced inflammatory responses were diminished by BBE as observed by a remarkable reduction in the levels of phosphorylated MAP Kinases, Erk1/2, p38, JNK1/2 and MKK4. Furthermore, BBE also reduced inflammatory mediators such as cyclooxygenase-2 (COX-2), prostaglandin E{sub 2} (PGE{sub 2}), and inducible nitric oxide synthase (iNOS) levels in UVB-exposed skin. Treatment with BBE inhibitedmore » UVB-induced nuclear translocation of NF-κB and degradation of IκBα in mouse skin. Immunohistochemistry analysis revealed that topical application of BBE inhibited the expression of 8-oxo-7, 8-dihydro-2′-deoxyguanosine (8-oxodG), cyclobutane pyrimidine dimers (CPD), proliferating cell nuclear antigen (PCNA), and cyclin D1 in UVB-exposed skin. Collectively, these data indicate that BBE protects from UVB-induced oxidative damage and inflammation by modulating MAP kinase and NF-κB signaling pathways. - Highlights: • Blackberry extract inhibits UVB-induced glutathione depletion. • Blackberry extract inhibits UVB-induced lipid peroxidation. • Blackberry extract inhibits UVB-induced myeloperoxidase activity. • Blackberry extract diminishes UVB-induced inflammatory responses. • Blackberry extract prevents skin from oxidative damage and inflammation by UVB.« less

Authors:
; ; ; ;  [1]; ;  [2]; ;  [1];  [3];  [1];  [2]
  1. Center for Research on Environmental Disease, University of Kentucky, 1095 VA Drive, Lexington, KY 40536 (United States)
  2. Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536 (United States)
  3. National Centre for Aquatic Animal Health, Cochin University of Science and Technology, Cochin (India)
Publication Date:
OSTI Identifier:
22465726
Resource Type:
Journal Article
Journal Name:
Toxicology and Applied Pharmacology
Additional Journal Information:
Journal Volume: 284; Journal Issue: 1; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0041-008X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANTIGENS; DAMAGE; EPITHELIOMAS; GLUTATHIONE; INFLAMMATION; IRRADIATION; LIPIDS; LYMPHOKINES; MICE; NITRIC OXIDE; OXIDATION; PHOSPHOTRANSFERASES; PROSTAGLANDINS; PYRIMIDINE DIMERS; SIGNALS; SKIN; STRESSES; ULTRAVIOLET RADIATION

Citation Formats

Divya, Sasidharan Padmaja, Wang, Xin, Pratheeshkumar, Poyil, Son, Young-Ok, Roy, Ram Vinod, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, Kim, Donghern, Dai, Jin, Hitron, John Andrew, Wang, Lei, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, Asha, Padmaja, Shi, Xianglin, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, and Zhang, Zhuo. Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signaling pathways in SKH-1 mice skin. United States: N. p., 2015. Web. doi:10.1016/J.TAAP.2015.02.003.
Divya, Sasidharan Padmaja, Wang, Xin, Pratheeshkumar, Poyil, Son, Young-Ok, Roy, Ram Vinod, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, Kim, Donghern, Dai, Jin, Hitron, John Andrew, Wang, Lei, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, Asha, Padmaja, Shi, Xianglin, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, & Zhang, Zhuo. Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signaling pathways in SKH-1 mice skin. United States. https://doi.org/10.1016/J.TAAP.2015.02.003
Divya, Sasidharan Padmaja, Wang, Xin, Pratheeshkumar, Poyil, Son, Young-Ok, Roy, Ram Vinod, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, Kim, Donghern, Dai, Jin, Hitron, John Andrew, Wang, Lei, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, Asha, Padmaja, Shi, Xianglin, Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, and Zhang, Zhuo. 2015. "Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signaling pathways in SKH-1 mice skin". United States. https://doi.org/10.1016/J.TAAP.2015.02.003.
@article{osti_22465726,
title = {Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signaling pathways in SKH-1 mice skin},
author = {Divya, Sasidharan Padmaja and Wang, Xin and Pratheeshkumar, Poyil and Son, Young-Ok and Roy, Ram Vinod and Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536 and Kim, Donghern and Dai, Jin and Hitron, John Andrew and Wang, Lei and Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536 and Asha, Padmaja and Shi, Xianglin and Department of Toxicology and Cancer Biology, University of Kentucky, 1095 VA Drive, Lexington, KY 40536 and Zhang, Zhuo},
abstractNote = {Extensive exposure of solar ultraviolet-B (UVB) radiation to skin induces oxidative stress and inflammation that play a crucial role in the induction of skin cancer. Photochemoprevention with natural products represents a simple but very effective strategy for the management of cutaneous neoplasia. In this study, we investigated whether blackberry extract (BBE) reduces chronic inflammatory responses induced by UVB irradiation in SKH-1 hairless mice skin. Mice were exposed to UVB radiation (100 mJ/cm{sup 2}) on alternate days for 10 weeks, and BBE (10% and 20%) was applied topically a day before UVB exposure. Our results show that BBE suppressed UVB-induced hyperplasia and reduced infiltration of inflammatory cells in the SKH-1 hairless mice skin. BBE treatment reduced glutathione (GSH) depletion, lipid peroxidation (LPO), and myeloperoxidase (MPO) in mouse skin by chronic UVB exposure. BBE significantly decreased the level of pro-inflammatory cytokines IL-6 and TNF-α in UVB-exposed skin. Likewise, UVB-induced inflammatory responses were diminished by BBE as observed by a remarkable reduction in the levels of phosphorylated MAP Kinases, Erk1/2, p38, JNK1/2 and MKK4. Furthermore, BBE also reduced inflammatory mediators such as cyclooxygenase-2 (COX-2), prostaglandin E{sub 2} (PGE{sub 2}), and inducible nitric oxide synthase (iNOS) levels in UVB-exposed skin. Treatment with BBE inhibited UVB-induced nuclear translocation of NF-κB and degradation of IκBα in mouse skin. Immunohistochemistry analysis revealed that topical application of BBE inhibited the expression of 8-oxo-7, 8-dihydro-2′-deoxyguanosine (8-oxodG), cyclobutane pyrimidine dimers (CPD), proliferating cell nuclear antigen (PCNA), and cyclin D1 in UVB-exposed skin. Collectively, these data indicate that BBE protects from UVB-induced oxidative damage and inflammation by modulating MAP kinase and NF-κB signaling pathways. - Highlights: • Blackberry extract inhibits UVB-induced glutathione depletion. • Blackberry extract inhibits UVB-induced lipid peroxidation. • Blackberry extract inhibits UVB-induced myeloperoxidase activity. • Blackberry extract diminishes UVB-induced inflammatory responses. • Blackberry extract prevents skin from oxidative damage and inflammation by UVB.},
doi = {10.1016/J.TAAP.2015.02.003},
url = {https://www.osti.gov/biblio/22465726}, journal = {Toxicology and Applied Pharmacology},
issn = {0041-008X},
number = 1,
volume = 284,
place = {United States},
year = {Wed Apr 01 00:00:00 EDT 2015},
month = {Wed Apr 01 00:00:00 EDT 2015}
}